HmsC Controls Yersinia pestis Biofilm Formation in Response to Redox Environment.

HmsC Controls Yersinia pestis Biofilm Formation in Response to Redox Environment.
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HmsC 响应氧化还原环境控制鼠疫耶尔森氏菌生物膜形成

DOI:
10.3389/fcimb.2017.00355
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发表时间:
2017
影响因子:
5.7
通讯作者:
Sun YC
Sun YC
中科院分区:
医学2区
文献类型:
--
作者:
Ren GX;Guo XP;Sun YC

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鼠疫耶尔森氏菌生物膜的形成受细胞内第二信使分子环二鸟苷酸(c-di-GMP)水平的控制,对于鼠疫从跳蚤到哺乳动物的阻断依赖性传播是重要的。HmsCDE是一个三方信号系统,它调节细胞内c-di-GMP水平以调节Y.鼠疫以前,我们发现Y。鼠疫菌生物膜的形成在还原环境中以hmsCDE依赖性方式被刺激。然而,HmsCDE感知氧化还原状态的机制仍然难以捉摸。使用dsbA突变体和添加Cu 2+来模拟还原和氧化周质环境,我们发现HmsC蛋白水平降低,并且HmsC-HmsD蛋白-蛋白相互作用在还原环境中减弱。此外,我们发现,蛋白质内二硫键是HmsC的关键,因为断裂降低蛋白质的稳定性,减少与HmsD的相互作用。我们的研究结果表明,HmsC可能在感知环境变化中发挥重要作用。
Yersinia pestis biofilm formation, controlled by intracellular levels of the second messenger molecule cyclic diguanylate (c-di-GMP), is important for blockage-dependent plague transmission from fleas to mammals. HmsCDE is a tripartite signaling system that modulates intracellular c-di-GMP levels to regulate biofilm formation in Y. pestis. Previously, we found that Y. pestis biofilm formation is stimulated in reducing environments in an hmsCDE-dependent manner. However, the mechanism by which HmsCDE senses the redox state remains elusive. Using a dsbA mutant and the addition of Cu2+ to simulate reducing and oxidizing periplasmic environments, we found that HmsC protein levels are decreased and the HmsC-HmsD protein-protein interaction is weakened in a reducing environment. In addition, we revealed that intraprotein disulphide bonds are critical for HmsC since breakage lowers protein stability and diminishes the interaction with HmsD. Our results suggest that HmsC might play a major role in sensing the environmental changes.
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